There was a reanalysis of data required to support the findings in
Development132,
133-142.

We have repeated the facial analysis reported in
Fig. 2 to provide the data
required to support some of the original findings of this study (see
Publisher's note). Our findings substantiate the original conclusions drawn
from Fig. 2 of a dose-related
genetic interaction between Disp1 and Shh alleles, and of the
function of Disp1 within Shh-producing cells. Some differences are
reported below, which might reflect slight differences in embryonic staging or
increased sensitivity of the whole-mount in situ hybridization procedure here.
Importantly, they do not alter the key conclusion that reducing Disp1
levels in Shh-producing cells results in a phenotype similar to that of
genetically matched embryos with reduced Disp1 activity throughout
the embryo. These data support the overall conclusions of the paper, and,
together with other data in the same report, support a model in which the
principal requirement for Disp1 activity is in Shh-producing cells.

Attenuating Disp1 activity specifically in Shh-producing cells
phenocopies Disp1 hypomorphic mutants. Attenuating Disp1
activity specifically in Shh-producing cells produced facial phenotypes that
resembled genetically matched embryos with Disp1 reduction throughout
the embryo. (A-E) External facial views of E18.5 embryos with the
indicated genotypes. (F-J) Whole-mount in situ hybridization with
Fgf8 probes to E10.5 embryos of the indicated genotypes. The
separation of Fgf8 expression domains in the frontal nasal processes
of wild-type embryos (bracket in F) reflects the normal development of midline
structures that were lost to varying degrees in embryos with attenuated
Disp1 and Shh activity (G-J). (K-O) Alcian Blue
(non-mineralized cartilage)-stained and Alizarin Red (mineralized cartilage
and bone)-stained head skeletal preparations of E18.5 embryos with indicated
genotypes. A variable loss was observed in both upper (arrow in K) and lower
(arrowhead in K) jaw structures, including the midline incisors. (P-Y)
Whole-mount in situ hybridization with (P-T) Ptch1 and (U-Y)
Shh probes to E9.5 embryos of the indicated genotypes. Ptch1
and Shh expression was evident in midline cell populations rostral to
the optic lobes in wild-type embryos (arrows in P and U). Their expression was
either markedly reduced or lost, depending on the specific combination of
Disp1 and Shh alleles (Q-T and V-Y). Ptch1 and
Shh expression was detected in the midbrain region (indicated by
arrowheads in P and U) of all genotypes, albeit at reduced levels.

The following text replaces the paragraph running from
p. 135 to
p. 137 (`In both genotypes...in
the Disp1 mutant background.')

Disp1Δ2/Δ2C; ShhCre/+ embryos in
which Disp1 activity was specifically knocked down in Shh-producing
cells have a facial phenotype with a narrowing of the face and reduction of
the premaxilla. However, the length of the snout is similar to wild type and
the mandibular incisors are not fused (Fig.
2A,C,K,M). Thus, the phenotype is, as expected, generally less
severe than that of the Disp1Δ2/Δ2;
Shh+/- embryos (Fig.
2B,L). The severity of the conditional phenotype is enhanced when
Disp1 activity is further lowered in
Disp1Δ2C/C829F; ShhCre/+ mice
(Fig. 2E,O) but the phenotype
is slightly weaker than that in Disp1Δ2/C829F (data
not shown) or Disp1Δ2/C829F; Shh+/-
embryos (Fig. 2D,N); the
tubular nasal process was shorter and the premaxillary bone was more
extensive. In a proportion of the latter, truncated fused mandibles lack
incisors (Fig. 2N); however,
mandibular fusion was not observed in Disp1Δ2C/C829F;
ShhCre/+ embryos. The slightly weaker facial phenotype seen at
term with each of the conditional removal combinations was evident at E10.5
when the distance between the Fgf8-expressing frontal-nasal processes
is compared by whole-mount in situ hybridization
(Fig. 2F-J). Variable weak
midline Shh expression was observed rostral to the optic stalk in
Disp1Δ2/Δ2C; ShhCre/+ embryos at
E9.5 (Fig. 2U-W). As expected,
this resulted in Ptch1 expression in adjacent nascent facial
structures (Fig. 2P-R). Small,
weak domains of Shh and Ptch1 expression were observed close
to the midline, localized to the region of the optic stalk in
Disp1Δ2C/C829F; ShhCre/+ embryos (not
readily visible in Fig. 2T,Y).
Only Disp1Δ2/C829F; Shh+/- embryos, the
strongest genetic combination, completely lacked Shh and
Ptch1 expression rostral to the diencephalon
(Fig. 2S,X).

The authors apologise to readers for any inconvenience caused by the
requirement to replicate these data and thank Mary Duah and Jill McMahon for
replicating the experiments, Joe Vaughan and Celia Shneider for help with data
acquisition, Renate Hellmiss for generating the figures and the journal
Development for encouraging the reanalysis.

In 2005, the McMahon laboratory reported that a re-examination of two
papers published by their group in Development
(Tian et al., 2004;
Tian et al., 2005a) had
revealed a duplication of Dr Tian's data in these papers. Following their
analysis, the authors announced, with regret, that they must retract Tian et
al. (2004), and this retraction
was published by Development in November 2005, along with their
apology to the editors and readership of the journal
(Tian et al., 2005b). With
respect to the second paper (Tian et al.,
2005a), the authors' review, overseen by the Committee on
Professional Conduct (CPC) for the Faculty of Arts and Sciences at Harvard
University, found that the principal conclusions of the paper were supported
by appropriate documentation but that the documentation for
Fig. 2 was inadequate,
requiring a replication of those data. The replicated data have been reviewed
by Development and are published in this Corrigendum.
Development and its publishers take very seriously issues relating to
the authenticity of data. We acknowledge the dedication and openness of the
McMahon laboratory in this matter, and the contributions of additional members
of the laboratory, not on the paper's authorship list, in repeating these
extensive experiments and data analyses for the Corrigendum.

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